Measles virus is a negative-strand RNA virus best known as the etiologic agent of the childhood rash. This virus also causes a block in cellular functions that results in immunosuppression. Measles virus is known to infect cells of the immune system and specifically suppress differentiated cellular activity. We have expanded existing observations about measles virus by studying the effects of this pathogen in antigen-specific T lymphocyte lines. Using this system, we have shown that measles virus suppresses antigen-specific proliferation. Our data indicates one mechanism of this suppression may be a decrease in interleukin-2 receptor alpha chain on the surface of infected cells. Further, we show that measles virus modulates cytokine elaboration by infected lymphocytes, resulting in an increase in interleukin-6 and interleukin-10, and a decrease in interleukin-4. Interleukin-2 and interferon-gamma levels were unchanged in supernatant fluids from infected cells. In order to explore the molecular mechanism underlying these viral effects on cells of the immune system, we have developed preliminary antisense techniques. We have demonstrated resistance to measles virus infection in transfected HeLa cells expressing antisense sequences to the ribosomal binding site of the measles virus nucleocapsid protein. Our control experiments establish that this inhibition of infection is specific for both the expressed sequence, and for the target virus. This work provides the foundation for the use of antisense techniques in lymphocyte systems as probes to determine the specfic intracellular mechanism of immunosuppression by measles virus.
University of Utah;
Molecular Mechansism; T lymphocyte Lines;
Measles virus; Immunosuppression;
University of Utah;
Relation-Is Version Of
Digital reproduction of “Modulation of immune responses by measles virus.” Spencer S. Eccles Health Sciences Library. Print version of “Modulation of immune responses by measles virus.” available at J. Willard Marriott Library Special Collection. QR6.5 1995 .B44.